In recent years, there has been persistent
promotion of a hypothesis by Gary
R Jackson that psoriasis is the result of widespread
subclinical insulin
resistance. Unfortunately, the deluge of references and connections he
has presented in thousands of often ad hominem posts do not sufficiently
support his theory. Combined with even more responses
correcting his many misconceptions and claims over the last four
years, this one-sided "debate" has been a persistent disruption
to the global psoriasis support
group. This is an attempt to put the known facts in perspective.

The problem with the theory is that it claims a universal cause and effect
from small statistical associations and variations in different populations.
Misleading exaggerations
have repeatedly been used in an attempt to magnify the true numbers. It has
been the basis for sometimes risky treatment recommendations by its
proponent, who more often pushes a controversial low-carb diet approach. Reports
of psoriasis improvement after dietary modification and associated weight
loss are more readily explained by other
factors.

Background

Diabetes
is a disease characterized by excessive glucose levels. Digestion, especially
of carbohydrates and sugars, increases glucose levels, which then decrease
as the glucose is metabolized. One of the key elements in glucose regulation
is insulin.

There are two classifications of diabetes. When insulin cannot be produced
by the pancreas, often because of an autoimmune attack or tumor, this is known
as Type I or Insulin Dependent Diabetes Mellitus (IDDM). When
available insulin cannot be utilized, this is Type II or Non-Insulin
Dependent Diabetes (NIDDM). There are specific risks
associated with having diabetes. Since undiagnosed or marginal glucose
regulation problems may put one at risk, it is good to be aware of potential
problems.

Subclinical NIDDM has
gotten a lot of attention because diabetes is reportedly reaching epidemic
proportions in western populations, yet may be easily preventable by dietary
changes. A hot topic in diet forums is Syndrome
X. The definition from the Stanford researchers' website says:

Hyperinsulinism to an emergency room doctor means excessive levels of insulin
associated with certain symptoms (weakness, hunger, sweating, staggering,
even convulsions or coma), but to a researcher it may simply mean noticably
elevated insulin levels.

Insulin resistance
can progress to NIDDM. At that point the pancreas cannot produce the amount
of insulin required to regulate glucose during digestion. Production of the
overloaded pancreas may eventually decline, leading to chronic hyperglycemia.
As the condition worsens the pancreas may be exhausted, and excess glucose
even generated (by the liver) during fasting between meals, at which point
it is likely to be detected during a medical exam.

Genetic factors for insulin receptor defects may be involved with insulin
resistance, and it is often associated with obesity. Excess glucose
is stored as body fat.

When the association was first published in the 1950's, the research consensus
was that diabetes had no causal relationship with psoriasis. Even if
these studies may have used a clinical definition of diabetes more severe
than the modern classification, that would be expected to emphasize the lack
of a direct connection to psoriasis, since a more extreme condition of elevated
insulin and glucose levels would be expected to have more evident side effects.
That isn't the case. There is a characteristic
array of skin conditions
associated with diabetes, but psoriasis is rarely mentioned among them.

A
statistical study of skin diseases that appear with diabetes reports that
the incidence of psoriasis related to NIDDM is approximately 4.6%, which is
only slightly higher than in the general population. Another counterpoint
to the IR theory of psoriasis is that NIDDM diabetics suffer most often from
skin infections, sometimes uncontrollable (9% in the above study), and they
are most serious in the legs and feet. Psoriatics, on the other hand, tend
to have fewer skin infections than the general population, most often opportunistic
fungi on the lesions.

Since psoriasis is not a disease of extreme insulin resistance, it is unlikely
that merely elevated insulin or glucose is the cause. Even if it were so,
then psoriasis would be expected to appear in conditions of hyperinsulemia.
Elevated insulin appears naturally in some populations, and in at least one
common condition.

During normal pregnancy, a state similar to insulin resistance arises as
the mother's body metabolism changes to meet the increased demands. This natural
state can actually send women who are already at risk for NIDDM into another
type of NIDDM known as gestational
diabetes. If psoriasis were caused by insulin resistance, it would be
expected to worsen during pregnancy. Just the opposite happens. A mother with
psoriasis often finds that it improves during pregnancy, and often later flares
again after the baby is born. This is more readily explained by her immune
system shifting from being suppressed so as not to reject the fetus, to then
delivering all the needed antibodies for the newborn baby's undeveloped immune
protection.

There are naturally variations in glucose metabolism among different populations.
Different enthicities have higher or lower insulin levels,
and women reportedly have overall higher levels than men. While these
are all natural "set points", the elevated insulin levels are of
most concern, because they put that population at greater risk of developing
insulin resistance and NIDDM. This is especially true among african, hispanic,
native american, and pacific island people. (The highest incidence in the
world is among the Pima
indian tribe, where over half the adults have diabetes.)

Again, if IR were a major contributing factor in psoriasis, it would be expected
to appear more often in populations with elevated insulin levels. Just the
opposite is true. Psoriasis is nearly absent in native americans (zero incidence
in a study of 26,000 south american indians), and relatively rare among african,
hispanic, and asian populations.

The accepted explanation for the variation in both psoriasis and diabetes
incidence is the genetic makeup. Psoriasis is a complex disease with multiple
genetic factors, and more genes are being discovered as research progresses.
Many autoimmune diseases are related to the HLA region on chromosome 6. There
are many different markers there that are often used to gauge disease risk
and HLA mapping is used to predict rejection/compatabiliy in organ donors.
People with active HLA-cw6 region are about 13 times more likely to have psoriasis
than the general population. People with HLA-dr3 or HLA-dr4 are at the highest
risk for IDDM. NIDDM, however, appears to be another genetically complex disease,
with ongoing
research in many candidate genes. Like psoriasis, environment also plays
a large part in insulin resistance.

It is important to note that population averages do not determine individual
variations. Given that about 3% of the general population has psoriasis, over
6% have (diagnosed) diabetes, and that the odds increase with age, it is not
at all uncommon for an older adult to have both.

One more notable example of insulin resistance is during treatment with corticosteroids
(glucocorticoids) such as prednisone. Steroids are commonly used in treating
skin diseases, and they are very effective as short term treatments for psoriasis.
Steroid use does carry some risk however, especially with oral use, systemic
absorption from injections, or excessive use of potent topicals. Some of the
side effects are similar to those of hyperinsulinism, such as rapid weight
gain, "moon face", and sweating. Perhaps a more immediate risk is
that of a "rebound" effect, where psoriasis flares when the steroids
are stopped abruptly, sometimes requiring hospitalization or converting to
a more difficult to treat form of pustular psoriasis.

If hyperinsulinism were responsible for psoriasis, inducing it with steroids
would not be expected to improve the condition. Nor would a rebound be expected,
since insulin metabolism settles back to normal within 48
hours after treatment is stopped. The rebound actually occurs because
of a lack of natural cortisol production from the adrenal glands, which have
shut down because the body recognizes the synthetic corticosteroids as excess
cortisol.

In the late 1970's, a team of italian NIDDM researchers became interested
in psoriasis as a risk factor, and conducted at least two clinical studies.
They found elevated insulin levels. In their 1977
study, they confirmed indications of insulin resistance fonud in earlier
studies, and formed a hypothesis that having psoriasis increases the risk
of developing NIDDM (not the other way around). In a later 1979
study, they conducted more detailed measurements, including the counting
of insulin receptors in liver cells. They determined that even when obesity
is not present, fewer receptors are found on average among psoriatics. They
also found a difference in receptor activity between obesity and psoriasis
which determined their conclusion:

"Finally, the results we have obtained appear to
confirm our first hypothesis, that psoriasis per se is a condition
initally responsible for endocrine-metabolic modifications."

Conclusions

The above facts cannot
be selectively ignored in an attempt to "prove" a pseudoscientific
theory of insulin resistance
as a cause for psoriasis. It has been repeatedly debunked from every
angle. Until further research uncovers some compelling new basis, the theory
needs to be set aside.

Given the various findings of elevated insulin levels among some people
with psoriasis, they should be aware that they may be at some risk
for developing Type II diabetes. The risk is not great, but at least one study
shows it may be double the risk found in the general population. Especially
since steroids are overprescribed in the treatment of psoriasis and psoriatic
arthritis, patients and doctors should
take extra care by watching for symptoms of insulin resistance.

A dietary change that has been recommended for both diabetes
and psoriasis
is to minimize saturated fat intake, while improving the ratio of "good"
fats by increasing the intake of omega-3 oils (abundant in
flax seed and in deep sea fish.) The "mediterranean
diet" with plenty of fresh fruits and vegetables is often recommended,
but "low-carb"
evangelists suggest eating more fat and fewer grains.

Many psoriatics who experiment with modifying their normal diet have found
that a particular food tends to trigger their psoriasis, but unfortunately
these effects are very individualized; What works for one person may do
nothing for the next.

The Journal of Clinical Investigation presented a series of perspective articles on insulin resistance.
The Full text of the articles are availiable online in both html and
Acrobat .pdf format. See the indices for:
July 15,
August 1, and
August 15

The Skin Page hosts all the dermatology
research tools used in this report.